Functional Neurological Symptoms After Mild Traumatic Brain Injury: A Scoping Review and Framework for Differentiating Functional and Organic Post-Concussion Presentations

1. Introduction

Mild traumatic brain injury (mTBI), commonly referred to as concussion, represents one of the most frequent neurological injuries worldwide, accounting for the majority of traumatic brain injuries across civilian, sporting, and occupational settings [1]. Although most individuals experience symptom resolution within weeks, a substantial minority develop persistent post-concussion symptoms (PPCS), including headache, dizziness, fatigue, cognitive complaints, emotional disturbance, and sensory or balance symptoms that may persist for months or years [2]. The pathophysiology underlying PPCS remains incompletely understood, and there is growing recognition that persistent symptoms are often poorly correlated with conventional markers of injury severity or structural brain damage. Persistent post-concussion symptoms (PPCS) refer to the persistence of physical, cognitive, and emotional symptoms beyond the expected recovery period following mild traumatic brain injury, typically operationalised as symptoms lasting longer than 4–12 weeks depending on diagnostic criteria [2].

Traditionally, persistent symptoms after concussion have been conceptualised as the downstream consequence of neurometabolic disturbance, microstructural injury, or prolonged physiological recovery. However, the non-specific nature of PPCS symptoms, their high prevalence in the general population, and their frequent overlap with psychiatric and functional disorders have long complicated causal attribution [3,4]. Symptoms commonly labelled as post-concussive—such as cognitive “brain fog,” fatigue, dizziness, and emotional lability—are not unique to mTBI and occur in a wide range of neurological and non-neurological conditions, as well as following non-head-injury trauma.

Early clinical studies highlighted that poor recovery after mTBI is often associated with factors other than injury characteristics alone [5]. Mooney and Speed (2001) demonstrated that psychiatric comorbidity, including depression, anxiety, dissociation, and conversion disorder, was strongly associated with prolonged recovery in a specialty mTBI clinic population, whereas objective neuropsychological impairment showed limited association with outcome [6]. Subsequent observational studies have reinforced the importance of affective, cognitive, and contextual factors in PPCS, including anxiety, fear-avoidance, maladaptive illness beliefs, and dissociative symptoms [7,8].

In parallel, Functional Neurological Disorder (FND) has been increasingly recognised as a common and disabling condition encountered in neurological practice. FND is characterised by genuine neurological symptoms arising from altered brain functioning rather than structural pathology, and diagnosis is based on positive clinical signs demonstrating internal inconsistency or incongruence with recognised neurological disease [3]. Functional symptoms span a wide range of phenotypes, including weakness, gait disturbance, tremor, sensory symptoms, speech and language disturbance, visual symptoms, and seizures. Cognitive symptoms have also been increasingly recognised, often conceptualised as Functional Cognitive Disorder (FCD) [9,10].

A growing body of evidence suggests substantial overlap between persistent symptoms after concussion and functional neurological presentations [11,12]. Systematic reviews have demonstrated a characteristic pattern of prominent subjective cognitive complaints with inconsistent or mild objective deficits across FND, fibromyalgia, and chronic fatigue syndrome, with similar profiles reported in mTBI and whiplash populations [13]. Broader systematic reviews of somatic symptom and related disorders further indicate that functional and somatic symptom burden is frequently elevated following mTBI, although methodological limitations and heterogeneity across studies preclude reliable incidence estimates [14].

Clinical reports increasingly describe functional neurological symptoms emerging after concussion. Case series and case reports have documented psychogenic gait disorders, functional weakness, visual conversion symptoms, dissociative presentations, and functional seizures complicating concussion recovery in both adult and pediatric populations [15,16,17,18]. More recently, a dedicated case series by Polich et al. (2024) described a broad spectrum of functional neurological phenotypes with symptom onset after concussion, many of which closely resembled PPCS, highlighting the diagnostic challenges inherent in routine clinical practice [19].

Among functional phenotypes, psychogenic non-epileptic seizures (PNES) have been particularly well studied in relation to head injury. Cross-sectional studies indicate that a history of traumatic brain injury—most commonly mTBI—is common in PNES populations and is associated with greater psychiatric comorbidity, trauma exposure, disability, and poorer functional outcomes [20]. Mechanistic syntheses have proposed that head injury may act as a precipitating or vulnerability factor for functional seizures through interactions between network-level disruption, stress responsivity, dissociation, and maladaptive learning processes, while emphasising that such associations are heterogeneous and not universally causal [21].

Beyond discrete diagnoses, emerging evidence suggests that persistent symptoms after concussion often reflect complex interactions between physical injury, psychological vulnerability, attentional processes, and contextual influences such as healthcare messaging and expectations. Narrative and conceptual reviews have argued against strict dichotomies between “organic” and “functional” pathology, proposing instead that concussion and FND may lie along a continuum of brain dysfunction shaped by injury, psychological factors, and social context [4,22,23].

Within this evolving landscape, Mavroudis et al. proposed the Functional Overlay Model, conceptualising persistent post-injury symptoms as arising from dynamic interactions between early injury-related changes and superimposed functional mechanisms [24]. In this framework, concussion acts as a salient trigger that may alter bodily sensations, cognitive efficiency, and emotional regulation, while functional processes—such as heightened symptom monitoring, altered predictive processing, and impaired sense of agency—may increasingly contribute to symptom persistence over time. The model offers a pragmatic way to understand mixed or evolving presentations, while acknowledging that organic and functional mechanisms may coexist [25].

Nevertheless, despite growing recognition of these interactions, the literature remains fragmented. Studies vary widely in design, definitions, populations, and outcomes, and few attempt to integrate functional neurological frameworks into concussion research in a systematic manner. Population-based incidence data for FND after mTBI are lacking, and there is limited synthesis across phenotypes, age groups, and clinical contexts. As a result, clinicians face ongoing uncertainty regarding how best to conceptualise, identify, and manage persistent symptoms after concussion.

The aim of the present study is therefore to provide a comprehensive scoping review and narrative synthesis of the evidence linking mild traumatic brain injury with functional neurological symptoms. By integrating data from systematic reviews, observational studies, case series, mechanistic papers, and emerging interventional research, this review seeks to clarify the scope of existing evidence, characterise the range of functional presentations reported after concussion, and identify key gaps that must be addressed to improve diagnosis, stratification, and treatment of patients with persistent post-concussion symptoms.

2. Materials and Methods

Study Design

This study was conducted as a scoping review with narrative synthesis, aiming to systematically identify, classify, and synthesise existing evidence examining the relationship between mild traumatic brain injury (mTBI), persistent post-concussion symptoms (PPCS), and functional neurological disorder (FND). The review focused on conceptual, clinical, mechanistic, and interventional literature, reflecting the heterogeneous nature of research at the intersection of concussion and functional neurological symptoms. As a scoping review, the objective was to map and synthesise heterogeneous evidence across conceptual, clinical, and mechanistic domains rather than to provide an exhaustive or quantitative systematic synthesis. Accordingly, study inclusion was guided by relevance and contribution to the conceptual framework rather than predefined numerical thresholds.

Search Strategy

A comprehensive literature search was conducted across major biomedical and psychological databases, including MEDLINE/PubMed, Embase, PsycINFO, and Scopus, from database inception to the most recent search date. The search strategy was intentionally broad to capture diverse study types relevant to this emerging interdisciplinary field. Search terms were developed to capture literature relating to mTBI and concussion in combination with functional neurological phenomena. Core search terms included combinations of:

• mild traumatic brain injury OR concussion OR post-concussion syndrome

AND

• functional neurological disorder OR conversion disorder OR functional cognitive disorder OR psychogenic non-epileptic seizures OR somatic symptom disorder

Reference lists of included articles and relevant reviews were manually screened to identify additional eligible studies.

Eligibility Criteria

Studies were eligible for inclusion if they met the following criteria:

• Involved human participants or provided clinically relevant conceptual or mechanistic analysis
• Examined functional neurological symptoms, FND, or related constructs in the context of mTBI or concussion
• Were published in peer-reviewed journals
• Were available in English

Eligible study designs included systematic reviews, narrative and conceptual reviews, mechanistic hypothesis papers, observational studies, case series, case reports, and interventional or neuroimaging studies. Conference abstracts, non-peer-reviewed reports, editorials without substantive analysis, and animal-only studies were excluded.

Study Selection

The database search yielded 120 records. After removal of duplicate records, titles and abstracts were screened for relevance. Following abstract screening, 32 studies were retained for full-text review. Full texts were assessed for eligibility based on the predefined inclusion criteria, resulting in the final set of studies included in the review. Following full-text assessment, 27 studies met inclusion criteria and were included in the final synthesis.

The study selection process is summarised using a PRISMA-style flow approach, with studies further classified by evidentiary role (systematic reviews, primary studies, mechanistic papers, and case-based evidence).

Data Extraction

From each included study, the following information was extracted:

• Author(s) and year of publication
• Study design and evidentiary category
• Population characteristics (where applicable)
• Type of functional neurological presentation (e.g., cognitive, motor, sensory, seizure-related)
• Key findings relevant to the relationship between mTBI, PPCS, and functional symptoms

Data extraction focused on qualitative synthesis rather than quantitative pooling, given the heterogeneity of study designs and outcomes.

Study Classification

Included studies were categorised into the following groups to facilitate synthesis:

• Systematic reviews
• Narrative or conceptual reviews
• Mechanistic or theoretical papers
• Primary observational studies
• Case series and case reports
• Interventional and neuroimaging studies

This classification informed the Results section and highlighted gaps in the current evidence base.

Data Synthesis

Given the heterogeneity of methodologies, outcomes, and study designs, a narrative synthesis approach was employed. Findings were synthesised thematically, focusing on phenomenological overlap between PPCS and FND, associated risk factors, mechanistic hypotheses, clinical implications, and emerging interventional evidence. No meta-analysis was performed due to the absence of sufficiently homogeneous quantitative data.

Risk of Bias Assessment

Formal risk-of-bias assessment was not performed, as the review incorporated diverse study designs including reviews, conceptual papers, and case-based evidence. Instead, methodological limitations and sources of bias within the existing literature are addressed narratively in the Discussion.

3. Results

Study Selection

The electronic database searches yielded 120 records. After removal of duplicates, titles and abstracts were screened, resulting in 32 studies underwent full-text review, of which 27 met inclusion criteria and were included in the final synthesis. Following full-text assessment, studies were excluded if they (i) did not address functional neurological symptoms in the context of mild traumatic brain injury (mTBI) or concussion, (ii) focused exclusively on moderate or severe TBI without relevance to concussion, or (iii) lacked primary data or substantive conceptual relevance (Figure 1).

After full-text screening, the final evidence base comprised systematic reviews, narrative and conceptual reviews, mechanistic hypothesis papers, primary observational studies, case series, case reports, and early interventional and neuroimaging studies, as summarised in Table 1. No population-based incidence studies of functional neurological disorder (FND) following mTBI were identified. Details of the study selection methodology are provided in the Methods section.

Overview of Study Types

The evidence base was heterogeneous and varied substantially in methodological strength. Systematic reviews and observational cohort studies provided the most robust data regarding associations between mTBI and functional neurological symptoms. In contrast, case reports and case series primarily served to illustrate clinical phenotypes and diagnostic challenges rather than establish causal relationships. Throughout the synthesis, higher weight was therefore given to systematic reviews and observational studies, while case-based evidence was interpreted cautiously as illustrative rather than confirmatory.

Two systematic reviews examined cognitive and somatic symptom profiles relevant to FND and mTBI [13,14]. Several narrative and conceptual reviews addressed diagnostic interfaces between concussion and FND [4,22,23]. One mechanistic hypothesis paper explored potential neurobiological vulnerability linking head trauma and functional seizures [21].

Primary data were provided by cross-sectional and clinic-based observational studies [6,7,8,20], supplemented by case series and case reports describing functional neurological presentations emerging after concussion [15,17,18,19]. Limited interventional and neuroimaging studies addressed treatment feasibility and neural correlates of functional cognitive disorder after concussion [26,27].

Systematic Reviews

Cognitive Symptoms and Functional Cognitive Disorder

Teodoro et al. (2018) conducted a systematic review of cognitive outcomes across functional neurological disorder, fibromyalgia, and chronic fatigue syndrome, including 39 studies of FND [13]. Across conditions, the authors identified a consistent pattern of marked subjective cognitive complaints (e.g., forgetfulness, concentration difficulties, mental fatigue) with inconsistent or mild objective neuropsychological deficits. When objective impairments were reported, they most commonly involved attention, processing speed, and susceptibility to distraction.

Importantly, the authors explicitly noted that similar subjective–objective discordance has been reported in patients with mild traumatic brain injury and whiplash, suggesting overlapping cognitive mechanisms across these conditions. Performance validity testing indicated that poor effort accounted for symptoms in only a minority of patients, arguing against widespread feigning as an explanation for persistent cognitive complaints.

Somatic and Functional Symptoms After mTBI

Jobin et al. (2025) performed a systematic review of somatic symptom and related disorders (SSRD) in mTBI, screening over 6,000 records and including 43 studies. Nine studies specifically examined functional seizures in relation to mTBI, while others evaluated somatization scales and clinician-diagnosed functional conditions [14].

Although the majority of included studies were rated as having unacceptable risk of bias, the acceptable-quality evidence consistently supported an association between mTBI and increased functional or somatic symptom burden. The authors highlighted the lack of high-quality prospective studies, and the absence of reliable incidence estimates for FND after mTBI.

Narrative and Conceptual Reviews

Phillips (2021) provided an expert narrative synthesis focused on FND in personal injury contexts [4]. The review emphasised that functional neurological symptoms commonly arise following minor accidents and injuries, including concussion, and cautioned against simplistic causal interpretations. Phillips highlighted the importance of diagnosing FND based on positive clinical signs, often demonstrated through inconsistency or distractibility, and stressed that such findings should not be equated with malingering.

More recent conceptual reviews proposed a continuum model linking concussion and FND, arguing that persistent post-concussion symptoms and functional neurological symptoms frequently overlap in phenomenology and underlying mechanisms [22,23]. These frameworks emphasised the role of expectations, illness beliefs, and healthcare interactions in shaping symptom persistence and recovery trajectories.

Mechanistic and Hypothesis-Driven Evidence

Popkirov et al. (2018) explored the relationship between head trauma and psychogenic non-epileptic seizures (PNES). Reviewing existing epidemiological and neurobiological evidence, the authors noted that a history of head injury is frequently reported in PNES populations [21]. They proposed that even mTBI, despite normal routine imaging, may result in subtle disruptions of long-range network connectivity, potentially increasing vulnerability to dissociation and functional seizures in predisposed individuals.

The authors emphasised that such neurobiological vulnerability does not replace established psychological models of PNES but may interact with mechanisms such as stress responsivity, maladaptive learning, and illness attribution.

Primary Observational Studies

Functional Seizures (PNES) and Prior mTBI

LaFrance et al. (2013) examined patients with EEG-confirmed PNES in a cross-sectional cohort. Of the 92 patients included, 41 (44.6%) reported a history of traumatic brain injury, and 73.2% of these met criteria for mild TBI [20].

Compared with PNES patients without TBI, those with prior TBI demonstrated higher disability rates, lower global functioning, and significantly greater psychiatric comorbidity. After adjustment for age and sex, prior TBI was associated with increased odds of major depressive disorder, post-traumatic stress disorder, trauma or abuse history, and cluster B personality traits [20]. These findings suggest that PNES patients with a history of mTBI represent a subgroup with increased psychosocial vulnerability and functional impairment.

Persistent Post-Concussion Symptoms and Psychiatric/Functional Factors

Mooney and Speed (2001) studied adults referred to a specialty mild TBI clinic, defining poor outcome as persistence of three or more post-concussive symptoms beyond three months [6]. Poor recovery was strongly associated with psychiatric comorbidity, including depression, anxiety disorders, and conversion disorder.

Dissociative symptoms were particularly prominent and robustly discriminated between good and poor recovery trajectories, with dissociation scores reported to predict outcome with high accuracy. In contrast, objective neuropsychological test abnormalities were not significantly associated with outcome, indicating that persistent symptoms were not primarily driven by measurable cognitive impairment [6].

Jobin et al. (2023) further demonstrated that, in patients with persistent post-concussion symptoms, greater functional neurological symptom severity was positively associated with higher post-concussion symptom burden, anxiety, and depression, reinforcing the interrelationship between functional symptoms and affective distress [8].

Case Series and Case Reports

Polich et al. (2024) reported a retrospective case series of 50 patients with clinician-confirmed FND whose functional neurological symptoms began after concussion [19]. Functional presentations were heterogeneous and included gait disturbances, functional seizures, speech and language symptoms, weakness, sensory symptoms, tremor, and visual or oculomotor disturbances.

Most patients exhibited multiple functional symptom types, and symptoms commonly overlapped with those typically labelled as persistent post-concussion symptoms, such as headache, dizziness, fatigue, and cognitive complaints [19].

Additional pediatric and adult case series and case reports described psychogenic gait disorders [15], conversion disorder with dissociative features [18], and functional motor deficits supported by advanced neurophysiological testing [17], illustrating the breadth of functional neurological presentations complicating concussion recovery across age groups.

Interventional and Neuroimaging Studies

Rioux et al. (2024) conducted a pilot randomised controlled trial evaluating the feasibility of cognitive-behavioural therapy tailored to functional cognitive disorder after concussion [26]. Both CBT and standard cognitive rehabilitation were well tolerated, with high adherence and credibility, although the study was not powered to detect differences in efficacy.

Westlin et al. (2025) examined structural brain measures in patients with functional cognitive disorder after concussion and reported no consistent group-level cortical or subcortical abnormalities compared with controls [27]. However, symptom severity and treatment response were associated with regional structural measures, suggesting that functional cognitive symptoms may relate to network-level vulnerability rather than focal injury.

Figure 2. Conceptual schematic illustrating the proposed functional–organic differentiation framework for persistent post-concussion symptoms. Following an initial concussion, early organic and physiological processes may predominate in the acute and subacute phases. Over time, three broad clinical trajectories may emerge: (1) predominantly organic post-concussion symptoms with gradual recovery, (2) predominantly functional neurological symptoms characterised by multisystem involvement and altered attentional, predictive, and interoceptive processes, and (3) mixed presentations in which organic and functional mechanisms coexist and interact. The framework emphasises dynamic evolution over time rather than a binary distinction between organic and functional pathology.

Figure 2. Conceptual schematic illustrating the proposed functional–organic differentiation framework for persistent post-concussion symptoms. Following an initial concussion, early organic and physiological processes may predominate in the acute and subacute phases. Over time, three broad clinical trajectories may emerge: (1) predominantly organic post-concussion symptoms with gradual recovery, (2) predominantly functional neurological symptoms characterised by multisystem involvement and altered attentional, predictive, and interoceptive processes, and (3) mixed presentations in which organic and functional mechanisms coexist and interact. The framework emphasises dynamic evolution over time rather than a binary distinction between organic and functional pathology.

Figure 3. Flow diagram outlining a pragmatic clinical approach to patients presenting with persistent symptoms following concussion. The pathway integrates assessment of injury-related factors with targeted screening for functional neurological features, psychiatric comorbidity, and dissociative symptoms. Based on clinical findings, patients may be stratified into predominantly organic post-concussion symptoms, predominantly functional neurological symptoms, or mixed presentations, guiding appropriate management and referral pathways. The model underscores the importance of positive diagnostic features, careful diagnostic communication, and early targeted intervention.

Figure 3. Flow diagram outlining a pragmatic clinical approach to patients presenting with persistent symptoms following concussion. The pathway integrates assessment of injury-related factors with targeted screening for functional neurological features, psychiatric comorbidity, and dissociative symptoms. Based on clinical findings, patients may be stratified into predominantly organic post-concussion symptoms, predominantly functional neurological symptoms, or mixed presentations, guiding appropriate management and referral pathways. The model underscores the importance of positive diagnostic features, careful diagnostic communication, and early targeted intervention.

4. Discussion

Principal Findings

This scoping review synthesises evidence from systematic reviews, observational studies, case series, mechanistic papers, and emerging interventional research to clarify the relationship between mild traumatic brain injury (mTBI) and functional neurological disorder (FND). Several consistent themes emerge. First, persistent post-concussion symptoms (PPCS) and functional neurological symptoms show substantial phenomenological overlap across cognitive, motor, sensory, visual, and seizure-related domains [3,4,19]. Second, functional neurological symptoms can clearly emerge after concussion, often presenting in forms indistinguishable from PPCS without targeted assessment [15,18,19]. Third, psychiatric comorbidity, dissociation, trauma exposure, and maladaptive attentional and illness-belief processes appear more strongly associated with symptom persistence than markers of injury severity or objective neurological impairment [6,7,8,20]. Finally, the current evidence base is dominated by clinic-derived, observational data, with a notable absence of population-level incidence studies or prospective mechanistic work [14].

Taken together, these findings support a shift away from simplistic injury-centric explanations of persistent post-concussion symptoms and toward integrative models that incorporate functional neurological mechanisms [4,22]. At the same time, they highlight the need for greater conceptual clarity in distinguishing functional symptoms from residual organic post-concussion pathology.

Functional Neurological Symptoms as a Contributor to PPCS

A central finding of this review is that functional neurological symptoms are not rare or incidental in post-concussion populations. Case series demonstrate that FND can present after concussion with a broad spectrum of phenotypes, including gait disturbance, functional seizures, speech and language symptoms, weakness, sensory symptoms, tremor, and visual or oculomotor abnormalities [19]. Similar presentations have been reported in pediatric and adult case series and reports, including psychogenic gait disorder [15], dissociative and conversion presentations in adolescents [18], functional motor weakness supported by advanced neurophysiological testing [17] and functional visual symptoms following concussion [16].

Importantly, many of these functional presentations overlap directly with symptoms commonly labelled as PPCS, such as dizziness, fatigue, headache, and cognitive complaints [3,19]. This overlap has important diagnostic implications. In routine clinical practice, persistent symptoms following concussion are often assumed to reflect delayed biological recovery, particularly when early imaging or neurophysiological findings are inconclusive. However, the evidence reviewed here suggests that in a meaningful subset of patients, persistent symptoms are better conceptualised as functional in nature, either emerging after the acute injury phase or coexisting with early organic effects [4,23]. Failure to recognise this may result in repeated investigations, prolonged rest prescriptions, and reinforcement of injury-focused illness beliefs, all of which may exacerbate symptom persistence.

Dissociation, Psychiatric Comorbidity, and Vulnerability Factors

Across study designs, psychiatric and dissociative factors consistently emerged as key correlates of persistent symptoms. Mooney and Speed (2001) demonstrated that dissociation strongly predicted poor recovery after mTBI, whereas objective neuropsychological impairment showed little association with outcome [6]. More recent studies have confirmed associations between functional neurological symptom severity, anxiety, depression, and trauma exposure in PPCS populations [7,8].

These findings align closely with broader FND literature, in which dissociation, affective dysregulation, and maladaptive attentional processes are recognised as central mechanisms [3,13]. Importantly, the present review reinforces that these factors are not merely epiphenomena of chronic illness but may actively shape symptom persistence and disability trajectories following concussion [4,14]. This has implications for early screening, prognostication, and treatment selection after mTBI.

Functional Seizures as a Model Phenotype

The relationship between mTBI and psychogenic non-epileptic seizures (PNES) provides a useful model for understanding broader functional symptom emergence after concussion. LaFrance et al. (2013) demonstrated that a history of traumatic brain injury—predominantly mTBI—is common in PNES populations and is associated with greater psychiatric comorbidity, trauma exposure, disability, and poorer global functioning [20]. Earlier work similarly identified head injury as a risk factor for PNES and adverse outcomes [6].

Mechanistic syntheses suggest that head injury may act as a salient precipitating event that interacts with pre-existing vulnerability, stress responsivity, dissociation, and maladaptive learning processes [21]. Importantly, PNES research illustrates how functional diagnoses can coexist with neurological histories without implying malingering or negating the reality of symptoms, a lesson directly applicable to PPCS more broadly [3,4].

Cognitive Symptoms and the Problem of “Brain Fog”

Cognitive complaints are among the most frequent and disabling persistent symptoms after concussion. The present review highlights strong parallels between cognitive symptoms in PPCS and those described in Functional Cognitive Disorder (FCD). Systematic review evidence indicates that subjective cognitive impairment often exceeds objective deficits, with attentional inefficiency, distractibility, and slowed processing rather than focal memory impairment predominating [13].

Empirical studies in mTBI populations support this interpretation. Picon et al. (2023) demonstrated that memory perfectionism, depression, and checking behaviours were strongly associated with functional memory symptoms after mTBI, whereas metacognitive efficiency did not significantly differ from controls. These findings challenge the assumption that persistent “brain fog” necessarily reflects ongoing brain injury and instead support models centred on altered attention, interoception, and expectation [13,24].

Emerging interventional evidence further supports the clinical relevance of these formulations. Rioux et al. (2024) showed that cognitive-behavioural therapy tailored to FCD after concussion is feasible and acceptable, while neuroimaging work suggests that symptom severity and treatment response relate more closely to network-level vulnerability than to focal structural damage [26].

Refining the Functional Overlay Model: from Overlap to Differentiation

Mavroudis et al. proposed the Functional Overlay Model to conceptualise persistent symptoms after concussion as arising from interactions between organic injury-related processes and functional mechanisms [24,25]. The present review supports the utility of this model as a heuristic framework, particularly in explaining mixed or evolving clinical presentations where functional and organic features coexist [19,23].

However, our findings also highlight the limitations of a purely “overlay” concept. While many patients may exhibit overlapping functional and organic features, the absence of clear differentiation risks two opposing errors: over-attributing symptoms to functional mechanisms when organic pathology remains clinically relevant, or persisting with an organic explanation when functional processes dominate [4,22].

Based on the evidence synthesised here, we therefore propose refining the Functional Overlay Model toward a functional–organic differentiation framework (Figure 2). In this framework, persistent post-concussion presentations can be broadly conceptualised into three non-mutually exclusive categories: (1) predominantly organic PPCS, (2) predominantly functional neurological symptoms emerging after concussion, and (3) mixed presentations in which organic and functional mechanisms coexist but contribute differentially to disability [13,24].

Clinical Implications

The findings of this review have several practical implications. First, concussion services should incorporate routine screening for functional neurological symptoms, dissociation, and affective distress in patients with persistent symptoms [4,8]. Second, clinicians should be trained to identify positive signs of FND and to communicate functional diagnoses in a validating, non-dualistic manner [3,4]. Third, early recognition of functional mechanisms may allow timely referral to targeted interventions, potentially reducing chronicity and disability [26] Figure 2).

Equally important, functional formulations should not be used to prematurely dismiss symptoms or deny care. Differentiation between functional and organic contributions requires careful longitudinal assessment, particularly in the subacute post-injury period [22,23].

Research Implications and Future Directions

The current literature is limited by methodological heterogeneity, reliance on clinic-based samples, and a lack of prospective studies. Future research should prioritise longitudinal designs examining symptom evolution after mTBI, incorporating functional neurological assessments alongside biomarkers, neuroimaging, and psychological measures. Population-based studies are needed to establish incidence and risk factors for FND after concussion. Interventional trials should stratify patients based on functional versus organic features to determine treatment-matching effects.

Strengths and Limitations of the Present Review

This review integrates diverse sources of evidence across disciplines, phenotypes, and age groups, providing a comprehensive synthesis of the mTBI–FND interface. However, conclusions are constrained by the quality and scope of available data. The absence of population-based incidence studies and the predominance of observational designs limit causal inference, and publication bias toward complex or refractory cases is likely.

5. Conclusions

Persistent symptoms after concussion frequently reflect more than delayed biological recovery. Functional neurological mechanisms appear to play a significant role in symptom persistence for a substantial subset of patients, often interacting with early injury-related changes. Recognising and differentiating functional symptoms from organic post-concussion pathology is essential to improving diagnosis, treatment, and outcomes. Refining conceptual models to move beyond overlap toward clinically meaningful differentiation represents a critical next step for the field.